Hemodynamic Disorders د. بنان برهان محمد ماجستير / هستوباثولوجي

The health of cells and tissue depends not only on an intact circulation to deliver oxygen and nutrients and to remove wastes but also on normal fluid balance (homeostasis). Normal homeostasis encompasses maintenance of vessel wall integrity as well as intravascular pressure and osmolarity within certain physiologic ranges.

 Edema  Hyperemia and congestion  Hemorrhage  Hemostasis and thrombosis  Disseminated intravascular coagulation  Embolism  Infarction  Shock Hemodynamic Disorders

Edema Approximately 60% of lean body weight is water, of which 2/3 is intracellular, 1/3 extracellular (mainly interstitial), only 5% of total body water is plasma Edema : means pathological accumulation of fluid in the interstitial tissue spaces or body cavities..

Collection of fluid in the different body cavities are variously designated: Peritoneal cavity → ascites (hydroperitoneum) Pleural cavity →hydrothorax pericardium→hydro pericardium anasarca → means severe & generalized edema with profound subcutaneous tissue swelling.

Nature of accumulated fluid: Transudate: this is serous (thin), protein poor fluid with specific gravity < 1.012, due to intravascular volume or pressure overload or reduced plasma protein (e.g. in heart failure, nephrotic syndrome). Exudate: it is protein rich fluid, specific gravity >1.020 due to ↑vascular permeability leads to escape of intravascular fluid with protein especially albumin. e.g. in inflammation.

There are 2 opposing factors which govern the movement of the fluid between vascular & interstitial spaces: hydrostatic pressure (intravascular pressure) encouraging the passage of fluid through the capillary wall to the extra vascular compartment. osmotic pressure (plasma protein) encourages the↑ retention of the fluid to the capillaries.

Normally, At the arterial end the hydrostatic pressure is greater than the osmotic pressure → fluid is forced out the capillaries, of the microcirculation. The reverse occurs at the venous end & the fluid is attracted into the vessels.

So the exit of fluid into the interstitium from the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end; a small residual amount of excess interstitial fluid is drained by the lymphatics, then to the blood stream via thoracic duct

Factors affecting fluid transit across capillary walls

Pathophysiology of edema(causes): Edema results from: 1. Increased hydrostatic pressure. 2. Reduced plasma osmotic pressure (hypoproteinemia). 3. Lymphatic obstruction. 4. Sodium and water retention. 5. Increased capillary permeability.

1-Increased hydrostatic pressure a.Generalized edema: It occurs most commonly in congestive heart failure (CHF), affecting Rt. ventricular function. The heart fails to pump the blood, that is received from the Rt atrium, this causes accumulation of blood that is reflect back into the systemic veins, as an increase in systemic venous pressure → generalized chronic venous congestion, this ↑ in hydrostatic pressure elicits edema formation.

CHF is associated with ↓ cardiac output and therefore reduced renal perfusion → stimulate renin –angiotensin -aldosterone axis, inducing Na+ and water retention by the kidney (secondary aldosteronism). This mechanism normally functions to ↑intravascular volume and improve cardiac out put to restore normal renal perfusion, however if the condition untreated the extra fluid load causes increased venous pressure and eventually ↑ edema.

B.Localized edema : As a result of impared venous return →↑ intravascular pressure → transudation of fluid e.g. **deep venous thrombosis(DVT)→edema restricted to the affected leg. **during pregnancy due to pressure on the veins by the gravid uterus → edema of the legs. **acute Lt ventricular failure →acute pulmonary edema.

2-reduced plasma osmotic pressure: (Hypoproteinemia) Reduced plasma osmotic protein→ movement of fluid into the interstitial tissue (edema). Reduced plasma volume→↓renal perfusion → 2'ry aldosteronism (Na+ and water retention) and edema precipitated by low protein is exacerbated by 2'ry Na+ and water retention.

Causes of reduced plasma oncotic pressure:: 1)protein malnutrition as in kwashiorkor. 2)Malabsorption 3) reduced albumin synthesis as in liver cirrhosis. 4)excessive loss of albumin e.g. nephrotic syndrome, also in protein – losing gastroenteropathy.

3-lymphatic obstruction : Impaired lymphatic drainage to area of the body →localized edema of the affected part (lymphedema). It is characteristically a non pitting edema. Causes: *inflammation: certain parasitic infestation e.g. filariasis →fibrosis of lymphatic vessels & L.N. of the inguinal region → edema of external genitalia &lower limbs (elephantiasis). * tumor invasion e.g. in carcinoma of breast → infiltration & obstruction of superficial lymphatics → edema of overlying skin → "peau d 'orange“. * resection of lymphatic channels or scarring related to surgery and radiation.

Lymphadema : (elephantiasis) non pitting edema of the legs

4. Sodium and water retention : e.g. acute renal failure and acute poststreptococcal glumerulonephritis. 5. increase capillary permeability : e.g. inflammation.

Morphology : Grossly : the edema is most easily recognized. Microscopically →edema fluid generally manifested as subtle cell swelling with clearing &separation of the extracellular matrix elements Although any organ or tissue may be involved, edema most commonly encountered in subcutaneous tissues, lungs and brain.

Subcutaneous edema: it can be: **dependent edema : edema more prominent in depended part of the body, the region with highest hydrostatic pressures (influenced by gravity) e.g. HF (Rt side HF) (in the legs when standing, in the sacrum when recumbent), **diffuse edema: Generalized and more severe edema, is usually due to renal failure or nephrotic syndrome.

Finger pressure over significantly edematous subcutaneous tissue will displace the interstitial fluid and leaving a finger-shaped depression (pitting edema)

Pulmonary edema: Is a common clinical problem and frequently follow Left side heart failure. The lungs are typically 2-3 times their normal weight. On sectioning frothy, sometimes blood-tinged fluid representing a mixture of air and edema fluid and extra-vasated RBCs.

Hyperemia and congestion Both terms indicate a local increased volume of blood in a particular tissue.

Hyperemia It is an active process. resulting from augmented blood flow due to arteriolar dilation. the affected tissue is redder than normal because of engorgement with oxygenated blood. e.g. - physiological as in skeletal muscle during exercise - pathological as in acute inflammation

Congestion : it is a passive process resulting from partial obstruction to the venous return from a tissue. the tissue has blue –red color (cyanosis) due to accumulation of deoxygenated blood in the affected tissue. Morphology: Grossly, the cut surface is hemorrhagic and wet. Microscopically, there is engorgement of capillaries by blood.

Hyperemia and congestion

General venous congestion: Where the whole venous return is impaired by chronic obstructions. Combined Rt and Lt sided heart failure(CHF) causes systemic congestion, Rt sided heart failure alone causes also systemic congestion but here the lungs are spared. Causes of Rt sided heart failure: 1.Lt sided heart failure, as it eventually leads to Rt sided heart failure. 2.Chronic obstructive airway disease such as emphysema, chronic bronchitis. 3.Pulmonary valve disease e.g. stenosis and /or incompetence.

Local venous congestion: Follows mechanical interference with the venous drainage from an organ e.g. ---pulmonary congestion occurs in mitral stenosis, Lt sided heart failure, systemic hypertension. ---thrombosis of the vein as in deep venous thrombosis (DVT). --- mechanical compression of the veins by tumor or bandage, strangulated hernias, volvulus of intestine venous congestion → edema then may → ischemic necrosis.

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